Candida albicans-infected oral epithelial cells augment the anti-fungal activity of human neutrophils in vitro
Candida albicans-infected oral epithelial cells augment the anti-fungal activity of human neutrophils in vitro
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DOI：
10.1080/13693780500064557
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发表时间：
2005-09-01
期刊：
影响因子：
2.9
通讯作者：
Kashleva, H
中科院分区：
文献类型：
--
作者：
Dongari-Bagtzoglou, A;Villar, CC;Kashleva, H
口咽念珠菌病（OPC）是免疫抑制患者中最常见的机会性感染。在OPC中，白色念珠菌持续存在于上皮内，引发炎症事件，通常不会引起侵入性感染。由于中性粒细胞在预防侵袭性感染中起着重要作用，并且由于它们仅在上皮细胞层内与微生物建立接触，因此我们检查了受真菌感染的口腔上皮细胞在体外增强嗜中性粒细胞介导的菌丝损伤的能力。我们发现在C.与基础中性粒细胞抗真菌功能相比，白色念珠菌感染的口腔上皮细胞上清液导致菌丝细胞代谢活性的显著更大抑制。中和抗IL-1 α抗体和IL-1受体拮抗剂可部分抑制这些上清液的抗菌丝活性。未感染口腔上皮细胞的对照上清液，以及C.白色念珠菌条件培养基对中性粒细胞抗真菌活性的影响不太明显，其不被这些细胞因子拮抗剂抑制。我们的结论是，口腔上皮细胞可以作为中性粒细胞抗菌丝功能的激活剂，这种作用可以部分归因于口腔粘膜细胞与病原体的相互作用过程中产生的免疫调节细胞因子。
Oropharyngeal candidiasis (OPC) is the most common opportunistic infection in immunosuppressed patients. In OPC, Candida albicans persists intraepithelially triggering inflammatory events, without generally causing invasive infection. Since neutrophils play an important role in preventing invasive infection and since they establish contact with the microorganisms only within the epithelial cell layer, we examined the ability of Candida-infected oral epithelial cells to augment neutrophil-mediated hyphal damage in vitro. We found that challenge of neutrophils with hyphal organisms in the presence of C. albicans-infected oral epithelial cell supernatants resulted in a significantly greater suppression of hyphal cell metabolic activity compared to basal neutrophil anti-fungal function. Antihyphal activity in response to these supernatants was partly inhibited by neutralizing anti-IL-1 alpha antibody and IL-1 receptor antagonist. Control supernatants from uninfected oral epithelial cells, as well as C. albicans conditioned-medium had a much less pronounced effect on neutrophil anti-fungal activity, which was not inhibited by these cytokine antagonists. We conclude that oral epithelial cells can act as activators of neutrophil anti-hyphal function, an effect that can be partly attributed to the generation of immunomodulatory cytokines during the interaction of oral mucosal cells with the pathogen.